5 articles
Rheumatoid arthritis is a systemic autoimmune disease in which persistent synovitis drives joint destruction and disability. Conventional biomarkers such as C-reactive protein and erythrocyte sedimentation rate are widely used to assess disease activity, but they fail to capture inflammation in a considerable proportion of patients and may be confounded by therapies such as interleukin-6 inhibition. Calprotectin (S100A8/A9, MRP8/14), a neutrophil- and monocyte-derived alarmin, has emerged as a potential biomarker reflecting the true inflammatory burden in rheumatoid arthritis. This review aimed to critically appraise the clinical and diagnostic value of calprotectin in adult rheumatoid arthritis, with emphasis on its relationship to disease activity, comparative performance against C-reactive protein and erythrocyte sedimentation rate, methodological aspects of measurement, and role in therapeutic monitoring.
We systematically reviewed studies published between 2010 and 2025 that investigated calprotectin in adult rheumatoid arthritis, focusing on serum, plasma, synovial fluid, and fecal measurements, and their associations with disease activity, imaging, treatment response, and outcomes. Additionally, seminal articles published before 2010 were included when they provided essential historical context or foundational theoretical data relevant to the understanding of calprotectin in rheumatoid arthritis. Pediatric and animal studies were excluded.
Serum calprotectin is consistently elevated in rheumatoid arthritis compared with healthy controls and correlates strongly with swollen joint counts, composite indices, and ultrasound-detected synovitis, often outperforming C-reactive protein and erythrocyte sedimentation rate. Synovial fluid calprotectin is markedly increased, reflecting local production and aggressive synovitis, while fecal calprotectin has limited utility except in cases of concomitant gastrointestinal involvement. Importantly, calprotectin levels remain reliable in patients receiving IL-6 inhibitors, where C-reactive protein is suppressed. High baseline calprotectin predicts radiographic progression and poor functional outcomes, whereas declining levels parallel therapeutic response to DMARDs and biologics. Recent studies suggest calprotectin may help identify patients at risk of relapse during apparent remission, though its predictive value for treatment response to TNF inhibitors appears limited.
Calprotectin is a sensitive biomarker of inflammation in rheumatoid arthritis, offering distinct advantages over traditional acute-phase reactants in detecting residual disease and guiding therapeutic monitoring. Standardization of assays, establishment of validated cut-off values, and large prospective validation studies are required before routine integration into clinical practice.
Rheumatoid arthritis (RA) is a chronic autoimmune disease affecting approximately 0.5% of the global population. It represents a major cause of disability, reduced quality of life, and healthcare burden. The prevalence of RA is rising, especially in older populations and in low-income regions.
A systematic literature search was performed in PubMed, ScienceDirect and Google Scholar for articles published between 2000 and 2025. Search terms included “rheumatoid arthritis”, “epidemiology”, “risk factors”, “economic burden”, and “healthcare disparities”.
RA prevalence ranges from 0.3% to 1.0%, with the highest values in Northern Europe (0.8–1.0%) and North America (0.7–0.9%), and the lowest in Africa (0.1–0.3%) and rural Asia (0.2–0.4%). Work incapacity has declined in several high-income countries, attributed to earlier diagnosis and the widespread use of disease-modifying antirheumatic drugs. Socio-economic status is a key factor for RA outcomes, with patients in the lowest income groups showing up to 50% higher disability rates. Other risk factors include female sex, HLA-DRB1 alleles, smoking, and environmental exposures. The economic burden is considerable, with direct and indirect costs disproportionately affecting low- and middle-income countries, where RA frequently results in early work disability.
RA causes disability and reduces quality of life. Its prevalence is rising worldwide, with higher detection and better outcomes in high-income countries, while low-income countries face underdiagnosis and limited access to modern therapies. Reducing these disparities requires stronger healthcare systems, early diagnosis, and affordable and accessible treatments.
Systemic rheumatoid vasculitis accounts for 1 to 5% of complications seen in rheumatoid arthritis, while autopsy studies report an average of 23% incidence. This enormous difference in numbers emphasizes the rate of misdiagnosis or underdiagnosis of systemic rheumatoid vasculitis. It mainly affects people with a median age of 65 years. It is particularly noteworthy, as systemic rheumatoid vasculitis has a high mortality and relapse rate. Also, the multifactorial aetiology: cytokines/immune cells and other particles determines clinical complexity of this type of angiitis.
A comprehensive literature search of articles published since 1996 was conducted using MEDLINE via PubMed and HINARI. The search included terms such as "rheumatoid vasculitis", "rheumatoid arthritis", and "endothelial dysfunction", focusing on mechanisms driving vascular damage. A total of 217 relevant sources were identified, including original studies, reviews, and book chapters. The study evaluated pathogenic factors like cytokines, immune complexes, and systemic inflammation, highlighting their roles in endothelial dysfunction and hypercoagulability.
The main pathogenetic factors in systemic rheumatoid vasculitis were immune complexes, cytokines (IL-6/TNF-α and IL-17), immune and blood cells (CD20/TH17/Platelets) and others (microparticles, blood rheology modifications). Even though, taken separately, those factors appear to have little to no impact on vascular endothelium, their synergistic effect lead to significant endothelial damage.
To conclude, each disease has its own pathogenetic factors which determine the natural course of this pathology. Understanding these mechanisms plays an important role for clinicians helping them to diagnose and effective treatment. Taking into consideration the relationships between specific factors in rheumatoid angiitis, we can make more specific decisions for its diagnosis and treatment. We can also use the pathophysiology of systemic rheumatoid vasculitis as a foundation for developing prevention measures.
Even if boron is not yet recognized as an essential element for the human body, its insufficient intake is considered harmful, especially for the osteoarticular system. A daily intake of at least 3 mg of boron can fortify bone mass and prevent the onset of osteoarthritis, rheumatoid arthritis, and osteoporosis. This research aims to assess the morbidity caused by rheumatoid arthritis and inflammatory polyarthropathies in the population from regions with different boron concentrations in deep drinking water of the Republic of Moldova.
Two full-length descriptive observational studies were conducted: one on osteoarticular morbidity caused by rheumatoid arthritis and inflammatory polyarthropathies (incidence and prevalence), and one on boron concentrations in deep drinking water (public wells and artesian wells). Following national regulations, the Republic of Moldova was divided into three distinct boron-related areas, and in each of them, the boron trend overlapped with the morbidity trend.
In the below-the-limit boron area, the research hypothesis was confirmed in two out of three districts, by overlapping osteoarticular morbidity with boron concentrations in deep drinking water and their trendlines. In the limit-level boron area, boron concentrations in drinking water do not appear to influence the studied osteoarticular morbidity in either district. In the above-the-limit boron area, unlike in previous research, trends for boron concentrations in public wells and artesian wells were opposite to those of the incidence and prevalence of rheumatoid arthritis and inflammatory polyarthropathies, confirming the research hypothesis.
Out of the three studied areas, the expected phenomenon of low morbidity and high boron concentrations, and vice versa, was observed in two below-the-limit boron districts and two above-the-limit boron districts. The results can be expanded upon in further research in the field.
Rheumatoid arthritis (RA) is the most common inflammatory disease of the joints, the prevalence of which is increasing in the population, leading to the emergence of new cases of the disease in young and middle-aged people, which has enormous medical and social significance. The study objective was to optimize the diagnosis and prediction of seronegative early rheumatoid arthritis outcomes by identifying the most significant clinical, laboratory and instrumental predictors of joint destruction.
The study includes 82 patients (22 men and 60 women), aged 17 to 70 years (average of 45.02±12.4 years), with the presence of articular syndrome (arthritis). All subjects were classified in the following groups: group I – 41 patients - 11 men and 30 women, whose average age was 44.46±13.36 years (average duration of the disease 6.0±2.9 months) with early seronegative rheumatoid arthritis (eRA), and group II consisted of 41 patients aged 45.55±11.12 years - 11 men and 30 women, with a diagnosis of seropositive rheumatoid arthritis (RA) (average duration of the disease of 6.8±3.7 months).
In the seronegative eRA group, the average Value of “prognostic index” (PrI) calculated from the data at the time of the initial survey was 5.67±1.72 points. PrI values in patients with transformation in RA within 1 year were significantly higher – 6.68±1.61, than without transformation in RA 4.52±0.96 points, p < 0.0001. At the same time, the values of PrI < 6 points were observed in 17 (20.7%) patients, PrI > 8 – in 25 (30.48%) patients, intermediate values (between 6 and 8 points) – in 40 (48.78%) patients, p < 0.001. Thus, in most patients with transformation in RA, the PrI values were more than 6 points.
In 53% of patients with seronegative RA, there is a transformation into seropositive rheumatoid arthritis during the first 18 months of the development of the disease. Features of early rheumatoid arthritis, in comparison with stabile RA are a polyarthritis presentation of the onset with damage to the joints of the hands, prolonged morning stiffness (more than 1 hour), moderate or high level of activity, the presence of productive synovitis and erosion during ultrasonography.